Analysis of cell death and repair pathway choice of DNA double-strand breaks caused by anti-cancer drug
| Project/Area Number |
24710061
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
Sakasai Ryo 金沢医科大学, 医学部, 助教 (10549950)
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| Research Collaborator |
SHIBATA Atsushi 群馬大学, 先端科学研究指導者育成ユニット, 助教 (30707633)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | DNA二本鎖切断 / 非相同末端連結 / 相同組換え / カンプトテシン / ユビキチン |
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| Outline of Final Research Achievements |
DNA double-strand breaks (DSBs) are severe DNA damage that can be caused by anti-cancer drug to kill cancer cells. Camptothecin (CPT) causes DSB via DNA replication in growing cells. However, cellular responses to DNA replication-mediated DSB (RM-DSB) had not been revealed. In this study, we analyzed regulatory mechanisms of RM-DSB repair pathway and discovered that UbcH5c, a E2 ubiquitin-conjugating enzyme, is involved in NHEJ pathway of RM-DSB repair leading to chromosomal aberration.
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Report
(5 results)
Research Products
(6 results)
